title: The mechanisms of cancer immunoescape and development of overcoming strategies.
abstract: Cancer-induced immunosuppression is a major problem as it reduces the anti-tumor effects of immunotherapies. In cancer tissues, cancer cells, immune cells, and other stromal cells interact and create an immunosuppressive microenvironment through a variety of immunosuppressive factors. Some cancer subpopulations such as cancer cells undergoing epithelial-mesenchymal transition and cancer stem-like cells have immunosuppressive and immunoresistant properties. The production of immunosuppressive factors by cancer cells is mechanistically attributed to oncogenic signals frequently activated in cancer cells, including the STAT3, MAPK, NF-κB, and Wnt/β-catenin signals, which are upstream events leading to immunosuppressive cascades. Moreover, some of these signals are also activated in immunosuppressive immune cells stimulated by cancer-derived factors and contribute to their immunosuppressive activities. Therefore, targeting these signals both in cancer cells and immunosuppressive immune cells may result in the restoration of immunocompetence in cancer patients and improve current immunotherapy.
authors.affiliation: Division of Cellular Signaling, Institute for Advanced Medical Research, 35 Shinanomachi, Shinjuku, Tokyo, Japan. beatless@rr.iij4u.or.jp.
authors.forename: Tomonori
authors.initials: T
authors.lastname: Yaguchi
authors.affiliation: Division of Cellular Signaling, Institute for Advanced Medical Research, 35 Shinanomachi, Shinjuku, Tokyo, Japan.
authors.forename: Hidetoshi
authors.initials: H
authors.lastname: Sumimoto
authors.affiliation: Division of Cellular Signaling, Institute for Advanced Medical Research, 35 Shinanomachi, Shinjuku, Tokyo, Japan.
authors.forename: Chie
authors.initials: C
authors.lastname: Kudo-Saito
authors.affiliation: Division of Cellular Signaling, Institute for Advanced Medical Research, 35 Shinanomachi, Shinjuku, Tokyo, Japan.
authors.forename: Nobuo
authors.initials: N
authors.lastname: Tsukamoto
authors.affiliation: Division of Cellular Signaling, Institute for Advanced Medical Research, 35 Shinanomachi, Shinjuku, Tokyo, Japan.
authors.forename: Ryo
authors.initials: R
authors.lastname: Ueda
authors.affiliation: Division of Cellular Signaling, Institute for Advanced Medical Research, 35 Shinanomachi, Shinjuku, Tokyo, Japan.
authors.forename: Tomoko
authors.initials: T
authors.lastname: Iwata-Kajihara
authors.affiliation: Division of Cellular Signaling, Institute for Advanced Medical Research, 35 Shinanomachi, Shinjuku, Tokyo, Japan.|Department of Obstetrics and Gynecology, Keio University School of Medicine, 35 Shinanomachi, Shinjuku, Tokyo, Japan.
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Nishio
authors.affiliation: Division of Cellular Signaling, Institute for Advanced Medical Research, 35 Shinanomachi, Shinjuku, Tokyo, Japan.
authors.forename: Naoshi
authors.initials: N
authors.lastname: Kawamura
authors.affiliation: Division of Cellular Signaling, Institute for Advanced Medical Research, 35 Shinanomachi, Shinjuku, Tokyo, Japan.
authors.forename: Yutaka
authors.initials: Y
authors.lastname: Kawakami
mesh_terms: D000818:Animals; D006801:Humans; D007108:Immune Tolerance; D007111:Immunity, Cellular; D007166:Immunosuppressive Agents / Q000276:immunology* / Q000378:metabolism; D007167:Immunotherapy; D009363:Neoplasm Proteins / Q000276:immunology* / Q000378:metabolism; D009369:Neoplasms / Q000276:immunology* / Q000378:metabolism / Q000628:therapy; D015398:Signal Transduction / Q000276:immunology*; D019139:Tumor Escape / Q000276:immunology*
chemical_list: D007166:Immunosuppressive Agents; D009363:Neoplasm Proteins